Selective inhibitors for eNOS have yet to be found, although several apparently potent and selective nNOS inhibitors have been identified using cell-free assays.
CD4+ and CD8+ T-cell subsets were identified using cell surface markers CD45RA and CD27 (Fig. 2b) and the frequency of platelet T-cell conjugates were determined by those T-cell subsets explatelet T-cellatelet reconjugates2b+.
In experiments measuring subcellular localization of fluorescent proteins, the nucleus was identified using cell-permeable nuclear markers (Hoechst 33342, Sigma).
Since inducible expression of c-Myc in antiestrogen-arrested cells can recapitulate many of the effects of estrogen on molecular endpoints related to cell cycle progression, the estrogen-regulated genes that were also targets of c-Myc were identified using cells inducibly expressing c-Myc.
For both adipogenesis and osteoblastogenesis, many key regulators have been identified using established cell model systems.
Targets have been identified using different cell-lines like BC-1, body-cavity-based lymphoma cell line (BCBL), BC-3, Lymphoblastoid, MSB1, Jijoye and others.
First, several potential small-molecule inhibitors of MYCN transcriptional function have been identified using a cell-based MYCN reporter gene assay [ 107].
After 4 days of incubation, viable cells were identified using a cell counting kit with WST-8 (Dojindo, Rockville, MD) and absorbance was tested at 450 nm colorimetrically.
Apoptotic cells were identified using a cell death detection kit (Roche Applied Sciences) using mouse monoclonal antibodies against fragmented DNA and histones according to the manufacturer's instructions.
Tregs were identified using the cell markers CD4, CD25 and the Treg specific transcription factor, Foxp3.
